The new coronavirus (SARS CoV 2) as a cause of dizziness in the COVID 19 pandemic

The pandemic of the coronavirus disease that began in 2019 (COVID 19) has posed a number of challenges for patients and for physicians. Its repercussions are changing rapidly, and our understanding of the disease itself is evolving.

How COVID 19 attacks the body

The pathogen (technically called “severe acute respiratory syndrome coronavirus type 2” or “SARS CoV 2”) belongs to a family of coronaviruses, which are single-stranded RNA viruses contained in a lipid bilayer envelope from which there protrude spike glycoproteins that comprise the “hooks” that let the viruses gain entry into host cells, where they replicate and propagate. These “hooks” attach particularly well to angiotensin-converting enzyme receptors (Ceccarelli, Berretta M Fau - Venanzi Rullo et al. 2020, Yan, Zhang et al. 2020) that are densely expressed in cells in the lungs, which is thought to be why some of the initial and most prominent symptoms of infection involve the respiratory tract, though unfortunately, the disease is not limited to the respiratory tract.

How COVID 19 attacks the brain:

The mechanism by which coronaviruses enter the central nervous system (CNS), and the factors that make specific people vulnerable to this, are incompletely understood (Dales 1995, Dube, Le Coupanec et al. 2018), though recent evidence (Baig, Khaleeq et al. 2020) has demonstrated that there are cells within the CNS that express angiotensin converting enzyme receptors — albeit at a lower density than in the lower respiratory tract. In any case, once the viruses have gained entry into the CNS, they appear capable of advancing by axonal transport (Dube, Le Coupanec et al. 2018).

Other members of the coronavirus family have long been known to invade the central nervous system, and have been found the brain/spinal cord tissue or the cerebrospinal fluid of patients suffering from a variety of neurological diseases, prominent among which are multiple sclerosis (Burks, DeVald et al. 1980, Salmi, Ziola et al. 1982, Hovanec and Flanagan 1983), Parkinson’s disease (Fazzini, Fleming et al. 1992), optic neuritis (Dessau, Lisby et al. 1999), encephalitis (Arabi, Harthi et al. 2015, Li, Li et al. 2016, Morfopoulou, Brown et al. 2016, Nilsson, Edner et al. 2020) and acute disseminated encephalomyelitis (Yeh, Collins et al. 2004). In some of these diseases (e.g., optic neuritis, encephalitis and encephalomyelitis) it is reasonable to suspect that the virus itself is the cause of the disease, while in other conditions (e.g., multiple sclerosis, Parkinson’s disease) it is unclear whether the virus has any causative role.

The accumulating evidence (Filatov, Sharma et al. 2020, Nath 2020, Poyiadji, Shahin et al. 2020) specifically about the virus causing COVID 19 suggests that it can affect the CNS similarly to other members of coronavirus family, though there are differences as well (Ceccarelli, Berretta M Fau - Venanzi Rullo et al. 2020), such as its apparent predilection to impair smell and taste (Gautier and Ravussin 2020, Giacomelli, Pezzati et al. 2020, Mao, Jin et al. 2020, Mermelstein 2020, Vavougios 2020). It is thus reasonable to consider whether it might also be the mechanism for other focal neurological manifestations, including the vertiginous disorders that we see in clinic — though to be clear, this disease is so new that there has not yet been adequate opportunity to study this in any systematic fashion.